5-MeO-DiBF
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5-MeO-DiBF (5-methoxy-N,N-diisopropylbenzofuranethylamine) is an emerging synthetic psychedelic of the benzofuran class. It is the direct structural analog of 5-MeO-DiPT, with oxygen replacing the indole nitrogen.[1] 5-MeO-DiBF is a presumed 5-HT₂A receptor agonist, producing its effects by activating serotonin receptors that alter sensory processing and cognition.[2]
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5-MeO-DiBF appeared on the research chemical market around September 2015,[3] likely developed as a legal alternative after its parent compound 5-MeO-DiPT was placed into Schedule I in 2004. It was first forensically identified in Slovenia in December 2015 and reported to the EMCDDA Early Warning System.[4] It remains one of the least-characterized psychoactive benzofurans in circulation, with only four publicly available experience reports.
Subjective effects include mild visual enhancement, tactile enhancement, sexual arousal, and mood elevation.[3] The experience is defined by its somatic emphasis — prominent sexual arousal and body awareness dominate a subdued cognitive and perceptual psychedelic profile, distinguishing it from more immersive tryptamines. Tremor and high sensitivity to set and setting are characteristic unsought effects.
No physical dependence has been documented, and rapid tolerance — consistent with the serotonergic psychedelic class — is expected to limit compulsive redosing.[2][5] The structural parent 5-MeO-DiPT produces persistent DNA damage in rodent brain tissue,[6] raising unresolved questions about whether the benzofuran modification preserves or alters this neurotoxic potential. No formal pharmacological characterization exists for this compound — the only published analytical data are NMR spectra of grey-market samples,[7] and the current understanding rests on structural analogy and a handful of user reports.
History[edit]
History
Market emergence
5-MeO-DiBF belongs to a family of benzofuran analogs created by replacing the indole nitrogen in established tryptamines with an oxygen atom. Its parent compound, 5-MeO-DiPT, was permanently placed into Schedule I in September 2004.[8][9] The benzofuran derivative appeared on the grey-market research chemical internet around September 2015, likely motivated by this scheduling.[3] No peer-reviewed synthesis paper has been published.
Forensic identification
The first definitive forensic identification occurred on December 23, 2015, by a laboratory in Slovenia, with formal notification to the EMCDDA Early Warning System.[1][4] Chapman (2017) published ¹H NMR spectral data for 5-MeO-DiBF purchased from grey-market vendors, confirming consistency with the labelled compound.[7] This remains the only published analytical characterization.
The name "5-MeO-DiBF" follows standard research chemical nomenclature: "5-MeO" for the 5-methoxy group, "Di" for the two isopropyl substituents, and "BF" for benzofuran. The alternative name "1-oxa-5-MeO-DiPT" makes the structural relationship explicit — "1-oxa" denotes the oxygen atom that replaces nitrogen in the parent compound's ring. Unlike its parent 5-MeO-DiPT, which earned the street names "Foxy" and "Foxy Methoxy" and developed a distinct cultural identity, 5-MeO-DiBF has no known slang names and negligible cultural presence.[10]
Chemistry[edit]
Chemistry
Structural class
5-MeO-DiBF is a substituted benzofuran-ethylamine — a class in which the indole ring of a tryptamine is replaced by a benzofuran ring, with oxygen substituting for the indole nitrogen. This swap preserves the planar aromatic scaffold and side-chain geometry of the tryptamine pharmacophore while eliminating the NH hydrogen-bond donor.[1] The compound carries a 5-methoxy group on the benzofuran ring and two isopropyl groups on the terminal amine, mirroring 5-MeO-DiPT.
5-MeO-DiBF is structurally distinct from the aminopropylbenzofuran (APB) compounds — 5-APB, 6-APB, 5-MAPB — which attach the aminoalkyl chain at a different ring position and function as monoamine releasers (entactogens) rather than direct serotonin receptor agonists.[11]
Molecular properties
| Molecular formula | C₁₇H₂₅NO₂ |
| Molecular weight | 275.4 g/mol |
The molecule is significantly lipophilic, predicting efficient passage across the blood-brain barrier and good central nervous system penetration.
Stereochemistry
5-MeO-DiBF contains no chirality centers. It exists as a single achiral species; stereoisomerism is not relevant to its pharmacological activity.
Physical properties
No published data exist for the melting point, solubility, crystal form, or environmental stability of 5-MeO-DiBF. The compound is presumed to be distributable as a solid (free base or hydrochloride salt) based on its molecular weight and structural class.
Pharmacology[edit]
Pharmacology
No published receptor binding, functional assay, or pharmacokinetic data exist for 5-MeO-DiBF. All pharmacological information in this section is inferred from the structural analog 5-MeO-DiPT and from class-level tryptamine pharmacology. inferred
Mechanism of action
5-MeO-DiBF is classified as a serotonin 5-HT₁A and 5-HT₂A receptor agonist based on structural analogy with 5-MeO-DiPT. No binding affinity or receptor occupancy data have been published for the benzofuran compound.
The closest pharmacological reference, 5-MeO-DiPT, binds more strongly to 5-HT₁A receptors than to 5-HT₂A in laboratory assays.[2] Despite this, the hallucinogenic effects of 5-MeO-DiPT are driven primarily through 5-HT₂A — selective blockade of this receptor abolishes the drug's behavioral signature in animal models, while blocking 5-HT₁A has no significant effect.[2]
5-MeO-DiPT also inhibits the SERT (SERT) with potency comparable to cocaine, blocking serotonin reuptake without reversing the transporter — distinguishing it from MDMA-type releasers.[12] Whether 5-MeO-DiBF shares this SERT-inhibiting property is unknown.
In animal models, 5-MeO-DiPT increases extracellular dopamine, serotonin, and glutamate across multiple brain regions.[6] This multi-neurotransmitter profile may contribute to the stimulant-like components of the experience. Psychedelic compounds generally interact with many receptor targets beyond their primary sites,[13] and 5-MeO-DiBF is expected to be no exception.
Pharmacokinetics
No human or animal pharmacokinetic data exist for 5-MeO-DiBF. inferred
The bulky N,N-diisopropyl groups shared with 5-MeO-DiPT are expected to confer oral bioavailability by reducing breakdown by monoamine oxidase — the enzyme that rapidly degrades simpler tryptamines like DMT and prevents their oral activity.[14][10] This steric protection explains why 5-MeO-DiBF is orally active without requiring an MAO inhibitor.
Genetic variation in the CYP2D6 liver enzyme, which is the major metabolic pathway for related tryptamines, represents a potential risk factor: individuals who metabolize drugs slowly through this pathway could accumulate higher-than-expected blood levels.[15] No data exist for plasma protein binding, half-life, or metabolite identity.
Neuroscience[edit]
Neuroscience
Where it acts
No direct neuroimaging or neurochemistry studies have been conducted with 5-MeO-DiBF. As a presumed serotonin 2A receptor agonist, it is expected to activate deep-layer neurons in the prefrontal cortex — the cellular trigger for psychedelic effects across the serotonergic class. Downstream, this typically disrupts the brain's sensory filtering system and loosens the default mode network, the circuit underpinning habitual self-referential thought. inferred
The structural analog 5-MeO-DiPT simultaneously elevates dopamine, serotonin, and glutamate across multiple brain regions in animal models,[6] and its SERT inhibition[12] adds a reuptake-blocking component absent from pure 5-HT₂A agonists like psilocin. If 5-MeO-DiBF shares these properties, its pharmacological profile would be a hybrid of direct receptor activation and transporter-mediated serotonin elevation.
Neurotoxicity and phenomenology
The mild psychedelic effects reported for 5-MeO-DiBF — visual enhancement without deep cognitive disruption — suggest weaker engagement of the cortical mechanisms that produce ego dissolution in more potent compounds. The disproportionately prominent sexual arousal, shared with parent compound 5-MeO-DiPT, may reflect preferential engagement of subcortical serotonergic circuits involved in sexual function.
The analog's documented neurotoxicity is a significant concern. 5-MeO-DiPT produces DNA strand breaks persisting up to 60 days in rat brain tissue, accompanied by dopaminergic damage.[6] Repeated adolescent exposure impairs learning tasks in a pattern consistent with lasting serotonergic disruption.[16] Whether the benzofuran modification alters these neurotoxic pathways remains an unanswered critical question.
- Does 5-MeO-DiBF produce measurable changes in default mode network integrity or global brain connectivity at typical human doses?
- Does the benzofuran modification alter the neurotoxic profile — specifically the persistent DNA damage and dopaminergic injury — established for 5-MeO-DiPT?
- What accounts for the roughly 5–10-fold potency reduction relative to 5-MeO-DiPT — reduced receptor binding, different metabolic processing, or both?
Subjective Effects[edit]
Subjective Effects
5-MeO-DiBF produces a psychedelic experience consistently described as mild — sexual arousal and tactile enhancement dominate the foreground, while cognitive disruption and visual distortion remain subdued even at higher doses. The experiential ceiling is notably low: the compound does not reliably produce the ego dissolution, deep perceptual restructuring, or immersive inner landscapes characteristic of more potent serotonergic psychedelics. Set and setting strongly modulate the experience, as with any psychedelic.
In comparative terms, 5-MeO-DiBF sits below its parent compound 5-MeO-DiPT in both potency and experiential depth, requiring roughly 5–10 times the dose and delivering a thinner phenomenological profile closer to a low-dose tryptamine experience than to the immersive psychedelia of psilocybin or DMT analogs.[3]
Effect Grid
At common doses (80–110 mg oral), 5-MeO-DiBF's characteristic profile becomes fully apparent. Visual enhancement is moderate: color alteration and color enhancement are noticeable, with mild visual drifting of surfaces and textures. The psychedelic headspace remains notably subdued compared to other tryptamines at equivalent experiential intensity — cognitive effects like analysis enhancement and conceptual thinking are present but faint.
The somatic signature dominates: a clear body high, moderate stimulation, and prominent sexual arousal enhancement — the latter disproportionately strong relative to the visual and cognitive components. Touch enhancement is marked. Temperature dysregulation and mild involuntary body movements (tremor) may occur. Nausea is possible but typically mild.
Time alteration is noticeable. Total duration is 4–6 hours. The experience is often described as "mild" relative to expectations set by the tryptamine class.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Light sensitivity · Holotropic state · Auditory enhancement · Visual drifting · Brightness alteration · Depth perception distortion · Environmental patterning · Sound sensitivity · Symmetrical texture repetition · Visual breathing · Auditory distortion · Tracers · After-images · Auditory misinterpretation · Peripheral vision distortion · Perspective distortion · Proprioceptive distortion · Spatial disorientation · Synesthesia · Visual diffraction · Visual haze / noise · Visual melting · Visual morphing · Visual acuity enhancement · Visual processing acceleration · Vestibular distortion · Visual magnification · Peripheral misidentification · Internal hallucinations · Object transformations · Auditory hallucinations · External hallucinations · Object activation · Perspective hallucinations · Visual recursion
Brightness alteration · Depth perception distortion · Environmental patterning · Sound sensitivity · Symmetrical texture repetition · Visual breathing · Auditory distortion · Tracers · After-images · Auditory misinterpretation · Peripheral vision distortion · Perspective distortion · Proprioceptive distortion · Spatial disorientation · Synesthesia · Visual diffraction · Visual haze / noise · Visual melting · Visual morphing · Visual acuity enhancement · Visual processing acceleration · Vestibular distortion · Visual magnification · Peripheral misidentification · Internal hallucinations · Object transformations · Auditory hallucinations · External hallucinations · Object activation · Perspective hallucinations · Visual recursion
Stimulation · Spontaneous body sensations · Body high · Sexual arousal enhancement · Nausea · Heart rate perception changes · Tactile euphoria · Tingling / electric sensations · Vibrations / buzzing · Involuntary body movements · Bodily lightness · Bodily pressures · Dizziness · Dry mouth · Insomnia · Muscle tension · Restlessness · Appetite suppression · Body schema distortion · Breathing alteration · Excessive sweating · Laughter fits · Trembling · Yawning · Abnormal heartbeat · Bruxism · Muscle relaxation · Vasoconstriction · Vomiting · Bodily dissociation
Sexual arousal enhancement · Nausea · Heart rate perception changes · Tactile euphoria · Tingling / electric sensations · Vibrations / buzzing · Involuntary body movements · Bodily lightness · Bodily pressures · Dizziness · Dry mouth · Insomnia · Muscle tension · Restlessness · Appetite suppression · Body schema distortion · Breathing alteration · Excessive sweating · Laughter fits · Trembling · Yawning · Bruxism · Muscle relaxation · Vasoconstriction · Vomiting · Bodily dissociation
Aesthetic enhancement · Introspection enhancement · Conceptual thinking · Thought acceleration · Cognitive euphoria · Cognitive flexibility · Immersion enhancement · Multiple thought streams · Openness enhancement · Memory suppression · Cognitive impairment · Creativity enhancement · Increased nature relatedness · Synchronicity · Thought loops · Analysis enhancement · Humor enhancement · Confusion · Memory fragmentation · Thought disorganization · Focus enhancement · Information processing enhancement · Motivation enhancement · Cognitive dysphoria
Cognitive euphoria · Cognitive flexibility · Immersion enhancement · Multiple thought streams · Openness enhancement · Memory suppression · Cognitive impairment · Creativity enhancement · Increased nature relatedness · Synchronicity · Thought loops · Analysis enhancement · Humor enhancement · Confusion · Memory fragmentation · Thought disorganization · Focus enhancement · Information processing enhancement · Motivation enhancement · Cognitive dysphoria
Catharsis · Simultaneous emotions · Anxiety suppression · Empathy enhancement · Dysphoria
Dysphoria
Flow state · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration
Identity alteration
Time cessation
Transpersonal visions · Death-rebirth sequence · Entity contact · Voidness
Timeline
Gradual emergence of somatic awareness — a subtle shift in body feeling without perceptual changes. No abrupt transition.
Building body sensations, early color enhancement, possible mild nausea. Sexual arousal may begin to emerge.
Maximum perceptual and somatic effects. Color enhancement, body high, and sexual arousal are most prominent. Cognitive headspace remains mild.
Gradual return to baseline. Residual visual disturbances and body sensations may persist as intensity fades.
Mild residual body sensation; baseline cognition restored. Subtle wakefulness may linger.
⚠ Avoid driving or operating heavy machinery for at least 6 hours after oral ingestion.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Safety
5-MeO-DiBF has no published toxicological data. All safety information is drawn from structural analogy with 5-MeO-DiPT and class-level serotonergic psychedelic pharmacology. The absence of adverse event reports does not constitute evidence of safety.
Toxicity
No lethal dose, therapeutic index, or toxic dose data have been published for 5-MeO-DiBF in any species. No human overdose case reports exist. A comprehensive review of novel psychoactive substance adverse events from 2017–2020, covering over 1,300 cases and 60 confirmed substances, did not include 5-MeO-DiBF.[17]
Neurotoxicity (analog data)
The structural parent 5-MeO-DiPT produces significant brain damage in rodent models. At doses of 5–20 mg/kg, it causes DNA strand breaks persisting up to 60 days, accompanied by decreases in dopamine-related brain chemicals suggesting damage to dopamine-producing nerve terminals.[6]
Repeated adolescent exposure produces lasting impairment in learning tasks, consistent with long-term serotonergic disruption.[16] Direct cell toxicity has been observed at high concentrations in laboratory cell cultures, independent of SERT expression.[12] safety citation needed
Whether 5-MeO-DiBF shares this neurotoxic potential cannot be determined without substance-specific studies.
Cardiovascular considerations
No cardiovascular data exist for 5-MeO-DiBF. By class effect, serotonin 2A receptor agonists can produce rapid heart rate, elevated blood pressure, and vasoconstriction. User reports noted tremor but no cardiovascular adverse events at documented doses.[18] safety citation needed
Psychological Risks
No controlled data address the psychological risks of 5-MeO-DiBF. By class inference from serotonergic psychedelics:
- Acute psychological distress: anxiety, panic, and temporary psychotic-like effects are possible at any dose, particularly in individuals with a predisposition to psychotic-spectrum conditions. The user-reported mildness of 5-MeO-DiBF may reduce but does not eliminate this risk.
- Hallucinogen persisting perception disorder (HPPD): No cases reported for 5-MeO-DiBF. The risk is theoretically present for any 5-HT₂A agonist.
- Psychosis: 5-HT₂A agonism carries inherent psychosis risk in vulnerable individuals. No cases documented for this compound.
Tolerance & Dependence
No published tolerance or dependence data exist for 5-MeO-DiBF. inferred
Rapid tolerance is a defining feature of serotonergic psychedelics, driven by receptor desensitization after agonist exposure. Community estimates place tolerance onset as immediate after ingestion, with full reset within approximately 7 days.[19] These values are extrapolated from the classical psychedelic pattern and remain unconfirmed for this compound.
Cross-tolerance with other serotonergic psychedelics — including LSD, psilocybin, and mescaline — is expected.[2][5]
5-MeO-DiBF is not expected to produce physical dependence or withdrawal. Tryptamines consistently demonstrate low abuse liability in laboratory models.[20]
Drug Interactions
No drug interaction studies have been conducted for 5-MeO-DiBF. All assessments are inferred from its predicted serotonergic mechanism. inferred
Serotonin syndrome risk
As a serotonin receptor agonist and putative serotonin reuptake inhibitor, 5-MeO-DiBF poses a theoretical risk of contributing to serotonin syndrome — a potentially life-threatening condition caused by excessive serotonin activity — when combined with other serotonergic agents.[21][22]
Tramadol: Classified as dangerous. Tramadol inhibits serotonin reuptake and has been implicated in fatal serotonin toxicity when combined with other serotonergic drugs.[23]
MAO inhibitors: Combining any serotonergic tryptamine with monoamine oxidase inhibitors (phenelzine, tranylcypromine, moclobemide) poses substantial risk of dangerous blood pressure spikes and severe serotonin syndrome.[23]
SSRIs and SNRIs: Risk exists through additive serotonergic effects. SSRIs may also blunt psychedelic effects through chronic receptor changes. safety citation needed
CYP2D6 inhibitors: If 5-MeO-DiBF is metabolized by CYP2D6 as predicted,[15] co-administration of potent inhibitors (fluoxetine, paroxetine, bupropion) could increase blood levels unpredictably.
Cannabis: Interaction profile unknown. No published data.
In the event of suspected serotonin toxicity: discontinue all serotonergic agents, contact emergency services immediately, and provide supportive care. Cyproheptadine (a 5-HT₂A antagonist) has been used as an antidote in clinical settings, though evidence for its efficacy remains limited.[24]
Contraindications
No published contraindications specific to 5-MeO-DiBF exist. The following are inferred from class-level serotonergic psychedelic pharmacology: inferred
- Personal or family history of psychotic-spectrum disorders (schizophrenia, schizoaffective disorder, bipolar I with psychotic features): 5-HT₂A agonism carries inherent psychosis risk. Absolute contraindication.
- Concurrent MAO inhibitor use: Risk of severe serotonin syndrome and dangerous blood pressure crisis. Absolute contraindication.
- Concurrent tramadol use: Elevated serotonin toxicity risk.[23] Absolute contraindication.
- Concurrent SSRI or SNRI use: Additive serotonergic risk; unpredictable effects. Relative contraindication.
- Concurrent CYP2D6 inhibitor use: Potential for elevated blood levels.[15] Relative contraindication.
- Pregnancy and lactation: No reproductive toxicity data exist. safety citation needed
- Severe heart conditions: Sympathomimetic effects (rapid heart rate, elevated blood pressure) pose theoretical risk. safety citation needed
Harm Reduction[edit]
Harm Reduction
Forms & Identification
5-MeO-DiBF has no independent analytical testing data from drug checking services, making verification of identity and purity especially important. Standard reagent testing can help distinguish the compound from more dangerous substitutions, but the absence of published reference reactions means results should be interpreted with caution.
Because the compound is extremely rare and poorly characterized, any sample acquired should be treated with heightened suspicion. Volumetric dosing from an accurately weighed stock solution is strongly recommended over estimating powder quantities by eye, given the lack of standardized formulations.
Guidelines
- Test every sample with at least two reagent kits before use
- Weigh doses with a milligram-precision scale — never estimate by eye
- Start at the lowest reported active dose and wait the full expected onset period before considering additional material
- Have a sober, trusted person present for first experiences
- Prepare the physical space: comfortable temperature, accessible water, quiet environment
- Avoid combining with other substances, especially on a first experience
- Eat lightly several hours beforehand to reduce nausea risk
- Set aside the full day — plan no obligations for at least 8 hours including aftereffects
Set & Setting
5-MeO-DiBF is reported to be highly sensitive to set and setting, with user accounts emphasizing that mental state and environment significantly shape the experience.[3] A familiar, comfortable, and private environment is advisable — particularly given the prominent sexual arousal effects, which may be unwelcome or disorienting in social settings.
A sober, trusted companion is recommended for first experiences. The compound's mild psychedelic ceiling does not eliminate the risk of unexpected anxiety or disorientation, especially given the near-total absence of dosing guidance from controlled studies.
Aftercare & integration. The mild experiential profile of 5-MeO-DiBF means most users will not require intensive integration. However, any psychedelic experience — even a subtle one — can surface unexpected emotional material.
In the days following use, note any shifts in mood, sleep, or perception. Journaling observations while they remain fresh can provide useful reference. If unusual perceptual phenomena (visual trails, pattern persistence) or mood disturbances last more than a few days, consult a healthcare professional. The near-total absence of safety data for this compound means any persistent aftereffects should be taken seriously.
Recovery & Support
5-MeO-DiBF carries low abuse liability by class inference, and compulsive use patterns have not been documented. If use of this or other psychoactive substances has become a source of distress or is interfering with daily functioning, support is available.
- SAMHSA National Helpline: 1-800-662-4357 (US, free, confidential, 24/7)
- Fireside Project: 62-FIRESIDE (psychedelic peer support)
- Global Drug Survey: highway.org.au (international resources)
Professional support from a therapist experienced with substance use or psychedelic integration can help contextualize difficult experiences.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable effects such as mild anxiety, nausea, or tremor during a 5-MeO-DiBF experience are not emergencies. Seek immediate help if any of the following occur: chest pain, seizure, loss of consciousness, extremely tachycardia that does not slow with rest, severe confusion or inability to communicate, or any sign of self-harm.
Immediate steps:
- 1. Call emergency services
- 2. Keep the person calm and in a safe position — seated or in the recovery position if vomiting or losing consciousness
- 3. Do not restrain them unless they are in immediate danger of harming themselves
- 4. Do not induce vomiting
- 5. Monitor breathing continuously
What to tell the dispatcher: Name the substance (5-MeO-DiBF, a synthetic benzofuran psychedelic), approximate amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
No specific reversal agent exists for serotonergic psychedelics. If serotonin syndrome is suspected (rigid muscles, high fever, agitation, rapid heart rate), cyproheptadine may be administered in a clinical setting.[24]
Legal Status[edit]
Legal Status
As of May 2026, 5-MeO-DiBF is not scheduled under the United Nations 1971 Convention on Psychotropic Substances. Its legal status varies by jurisdiction.
In the United States, it is not explicitly listed under the Controlled Substances Act. However, the Federal Analogue Act may apply given its structural similarity to 5-MeO-DiPT, which has been Schedule I since 2004.[8][9] In the United Kingdom, blanket psychoactive substance legislation covers it regardless of specific scheduling.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not explicitly scheduled | Federal Analogue Act may apply if sold for human consumption; 5-MeO-DiPT is Schedule I (since September 2004).[9] No prosecution under FAA for 5-MeO-DiBF has been documented. citation needed |
| United Kingdom | Prohibited under Psychoactive Substances Act 2016 | Illegal to produce, supply, or import; not specifically listed under Misuse of Drugs Act 1971[1] |
| Canada | Not a controlled substance | Not listed under the Controlled Drugs and Substances Act as of 2025; no catch-all provision for tryptamines[1] |
| Armenia | Controlled substance | Listed as a controlled substance as of 2022[1] |
| European Union | Not scheduled EU-wide | Formally notified to the EMCDDA Early Warning System in December 2015;[4] individual member states may have national controls |
| Australia | Unverified | Specific scheduling under the Poisons Standard (SUSMP Schedule 9) not confirmed citation needed |
| Germany | Unverified | Status under the Neue-psychoaktive-Stoffe-Gesetz (NpSG) or BtMG not confirmed citation needed |
Analog act considerations
In the United States, the Federal Analogue Act (21 U.S.C. § 813) provides that any substance "substantially similar" in chemical structure or pharmacological effect to a Schedule I or II substance may be treated as controlled if intended for human consumption. 5-MeO-DiBF differs from Schedule I 5-MeO-DiPT only in the indole-to-benzofuran ring substitution.[8] This applicability has not been tested in court for 5-MeO-DiBF.
references
- [1]
- [2]
- [3]
- [4]
- [5] ^abGlatfelter GC, Naeem M, Pham DNK, Golen JA, Chadeayne AR, Manke DR, Baumann MH (2023) Receptor Binding Profiles for Tryptamine Psychedelics and Effects of 4-Propionoxy-N,N-dimethyltryptamine in Mice — ACS Pharmacology & Translational Science doi:10.1021/acsptsci.2c00222
- [6]